Agents, currently used to stimulate the failing heart are limited by their toxic effects on the heart or by deleterious side effects on the peripheral circulation. For example, although the cardiac glycosides are myocardial stimulants and can restore the failing heart, they do so at doses very close to those which produce toxic symptoms of cardiac arrhythmia, nausea and vomiting. The use of sympathomimetic agents are limited by associated arrhythmia, tachycardia, tachyphylaxis or altered peripheral resistance.
The compound of this invention exhibits valuable pharmacological properties. It primarily affects the contractile force of the heart muscle. In particular, it has a potent cardiotonic action on the cardiac muscle of different animals in vivo and in vitro but does not have any demonstrable effect on the blood pressure, heart rate and vascular smooth muscle. The compound also causes a positive inotropic effect on atria under severe temperature stress, anoxia and in the presence of low Ca.sup.++ concentrations. The cardiac glycosides are ineffective under these stressful conditions. These specifics positive inotropic properties of AP-A make it useful in the treatment of congestive cardiac failure.
Congestive heart failure results when the heart pumps less blood than is required by the metabolic demands of the body. The objectives of therapy are to restore the balance of supply and demand for blood. This can be achieved through the use of the instant cardiotonic agent which improves myocardial contractility and influences cardiac output to meet the demands of the body.